Lipoprotein Lipase Gene Polymorphism and Lipid Profile in Coronary Artery Disease
Autor: | Belhhan Akpinar, Belgin Süsleyici Duman, A. Sevim Büyükdevrim, Mustafa Güden, Penbe Cagatay, Çavlan Türkoğlu, Demet Günay, Anastassiia Vertii, Esranur Dak |
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Rok vydání: | 2004 |
Předmět: |
Male
medicine.medical_specialty Genotype Turkey Coronary Disease Comorbidity Biology Pathology and Forensic Medicine Coronary artery disease chemistry.chemical_compound Gene Frequency Risk Factors Internal medicine medicine Humans Genetic Predisposition to Disease Lipase Deoxyribonucleases Type II Site-Specific Genetics medicine.diagnostic_test Triglyceride Smoking Intron Lipid metabolism General Medicine Middle Aged medicine.disease Introns Lipoproteins LDL Lipoprotein Lipase Medical Laboratory Technology Cholesterol Endocrinology Amino Acid Substitution chemistry biology.protein Female lipids (amino acids peptides and proteins) Lipid profile Polymorphism Restriction Fragment Length Chylomicron |
Zdroj: | Scopus-Elsevier |
ISSN: | 1543-2165 0003-9985 |
Popis: | Context.—Lipoprotein lipase (LPL) plays a central role in lipid metabolism, hydrolyzing triglyceride in chylomicrons and very-low-density lipoproteins. The PvuII polymorphic variant of LPL gene is common and might affect risk of coronary artery disease (CAD). Objective.—Our aim was to determine whether LPL– PvuII polymorphism can be considered to be an independent risk factor or a predictor for CAD in Turkish subjects. Design.—We used polymerase chain reaction and restriction enzyme digestion to determine the distribution of the previously described C→T transition that causes a PvuII polymorphism in intron 6 among healthy blood donors of Turkish origin and among angiographically confirmed CAD patients with comparable ethnic backgrounds. Results.—For the PvuII genotypes, within the CAD group (n = 80), the +/− genotype was found in 39 individuals (48.8%), whereas 25 (31.3%) carried the +/+ genotype, and 14 (17.5%) carried the −/− genotype. Within the control group (n = 49), the −/− genotype was found in 19 individuals (38.8%), 16 (32.7%) carried the +/− genotype, and 14 (28.6%) carried the +/+ genotype. The genotype frequency distribution was significantly different (P = .049) in the CAD and control study groups. The most frequent genotype among CAD patients was +/−; this genotype was more frequent in patients than in control subjects. However, the −/− genotype was more prevalent in the control group. Lipoprotein lipase–PvuII polymorphism was found to be associated with fasting total cholesterol and low-density lipoprotein cholesterol levels. The +/+ genotype was found to have higher levels of total cholesterol and low-density lipoprotein cholesterol in both the CAD and control groups. Conclusion.—There was a difference in the distribution of LPL–PvuII genotypes between the healthy subjects and the patients with CAD. Lipoprotein lipase–PvuII polymorphisms were not detected as independent risk factors for CAD in this study group, but had associations with lipid levels. |
Databáze: | OpenAIRE |
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